Comprehensive Guide to Heart Conduction and ECG Fundamentals

 Hello everyone.   Welcome to this online  course on Electrocardiogram.   I am Dr. M. Anbarasi, Professor of Physiology  from Chettinad Hospital and Research Institute.  

In this very first video lecture, we are going  to see about the basic conduction of the heart.   This is very important in understanding the  principles of electrocardiography.    In this lecture, I am going to take you  all through the functional anatomy of the  

conducting system of the heart; the role of gap  junctions; the various cardiac potentials, namely   the pacemaker potential and the ventricular action  potential; how this wave of excitation is spread   to the entire myocardium; and then and there, we  will be seeing about the control of excitation  

and conduction in the heart.  In the first section,   we are going to see about the  conducting system of the heart.   This is nothing but the electrical pathway  that lead on to atrial and the ventricular  

contraction. The electrical activity is produced  by one group of cells that leads on to the   mechanical phenomenon that is your ventricular  muscle contraction. Now, the cardiac cells   are classified based on the function as well  as based on the speed of conduction.   

Based on the function, the cardiac cells are  classified as pacemaker cells and contractile   cells. The SA node, AV node, bundle of His  and its branches and the Purkinje fibre system   forms the pacemaker cells, whereas the atrial  and the ventricular cardiac myocytes form the  

contractile cells. Based on the speed of  conduction, the cardiac cells are classified as   slow fibres and fast fibres. The SA node  and AV node are the slow fibres, whereas the   Purkinje fibre system, atrial and the ventricular  myocytes are the fast conducting fibres.   

In this picture, we are seeing the conducting  system of the heart. You can see here;   this is a structure present in the roof of  the right atrium; this is the SA node. There   is another structure in the floor of the right  atrium, which is called as the AV node. These two  

structures are connected to each other by means  of 3 internodal tracts namely the anterior, middle   and the posterior internodal tract.  Also, a branch of the anterior internodal   tract also goes to the left atrium to excite the  left atrium. The AV node continues as His bundle  

which very soon branches into right branch and the  left branch. The left branch again branches into   anterior fascicle and the posterior  fascicle; both the branches then go and   merge with the Purkinje fibre system. This  is the conducting system of the heart.   

Now, let us see the pacemakers of the  heart. What is this pacemaking activity?   This is nothing but the spontaneous time  dependent depolarisation of the cell membrane   that may lead on to an action potential  in an otherwise resting cell. The word  

time dependent is very important here, because  this depolarisation occurs at regular intervals.   And this regular interval or spacing is the one  which is deciding the rhythm of the heartbeat.    Now, there are different cells of pacemaker cells  in the heart. The fastest pacemaker is usually  

setting the heart rate. The fastest pacemaker  is the one which has got the highest frequency.   So, in that order, if we can see, the SA node, the  sinoatrial node has got the frequency of 60 to 100   beats per minute. This is the primary pacemaker  of the heart. Next is the AV node. It has got the  

frequency of 40 to 60 beats per minute, which  is followed by the Purkinje fibres which is   capable of producing the electrical activity  at a rate of 20 to 40 beats per minute.    Let us see the sinoatrial node. It is located at  the wall of the right atrium, just below and to  

the right of the opening of superior vena cava.  When compared to the entire heart, this SA node   forms the smallest electrical region, but this has  got the fastest pacemaking activity at a rate of   60 to 100 beats per minute. The rhythm produced by  the SA node is called as normal sinus rhythm.   

Now, this inherent or intrinsic pacemaker activity  also called as automaticity or auto rhythmicity   is subjected to sympathetic and parasympathetic  influence. The sympathetic activity increases   the automaticity by acting on the beta receptors,  whereas the parasympathetic activity decreases the  

SA nodal activity by acting on the Muscarinic  2 receptors, that is M 2 receptors.    Also, this SA nodal cells or the targets for the  therapeutic agents which try to modulate the heart   rhythm; for example, the calcium channel blockers,  beta adrenergic blockers act on the channels  

present in these SA nodal cells  to modulate the heart rate.    Next we will see about the internodal  tracts of impulse conduction.   As we saw in the previous picture, the SA  node generates the pacemaker potentials,  

which will be carried to the AV node via these  3 internodal tracts, the Anterior or Bachmann's,   Middle or Wenckebach, Posterior or  Thorel's bundle. Apart from that,   a branch of Bachmann's bundle also reaches the  left atrium to excite the left atrial tissues.  

Now, apart from these physiological internodal  tracts, the general excitation can also spread   from cell to cell in the atrium via a specialised  structure called as the gap junctions.    Next in the order of conducting  system is the atrioventricular node,  

which is located in the anteroinferior part  of the interatrial septum above the opening of   coronary sinus. This particular area is called  as triangle of Koch. Compared to the SA node,   this AV node has got fewer pacemaker cells,  and this also continuous as the bundle of His.  

The main function of this AV node is  that it acts as a reserve pacemaker;   that is, when the SA node fails, this AV node  will take up its position of pacemaker.    And this conducts the action potential from the  atria to the ventricles in a unidirectional way.  

This also mediates a very important  phenomenon called as AV nodal delay,   which we will be discussing shortly.  Next, the AV node continues as the bundle of His   and which merges into the Purkinje system  of fibres. This bundle of His branches into  

right branch and the left branch. The left branch  once again branches into anterosuperior fascicle   and posteroinferior fascicle. The right  branch supplies the entire right ventricle,   whereas the anterosuperior fascicle supplies  the anterior wall of the left ventricle,  

and posteroinferior fascicle supplies the  posterior wall of the left ventricle.    In the next section, we are going to see about  the cardiac muscle and its properties. Like   skeletal muscle, cardiac muscle is also a striated  muscle with nucleus and many active mitochondria,  

but then, the cardiac cells  they branch and interdigitate.   The most important feature of the cardiac  muscle is that the adjacent cardiac muscles,   they are united by means of a special  structure called an intercalated disc.  

See, this is a histological picture of the cardiac  muscle The adjacent muscles when you expand,   you can see the adjacent plasma membrane; plasma  membrane of the adjacent cardiac cells, they   approximate each other in forming the specialised  structure called as intercalated disc.   

Now when the SA node is generating the  action potential, the wave of depolarisation   is spread from one cell to another  via the intercalated disc.    You can see, the intercalated disc is actually  the plasma membrane, which lie in close proximity  

with the adjacent cell's plasma membrane. They are  bound tightly with, by means of desmosomes. This   is the desmosome. And then, in the area where  the plasma membranes approximate each other,   there is a special channel called as gap  junctions, which are the low resistance  

bridges across which the electrical current  flow from one cell to another cell.    Consider the cells A, B, C and D are  all the adjacent myocardial cells bound   to each other by means of this gap junctions, this  yellow structure. And you can see, the cells are  

all in the resting stage as is denoted by the  negative ions lining the interior of the cell,   while positive ions are lining the exterior of the  cell. There are membrane channels present in the   cells, which can conduct the positive ions.  Now, when the cell A is excited, what happens,  

a wave of depolarisation will spread from A to B.  This will cause increase in the positivity in the   cell B, which will open up the membrane channels  and positive ions flow into the cell B. This will   further enhance a positivity or depolarisation  in the cell B which will be conducted from B to  

C by other gap junctions. And the cell C will  now have increased depolarisation in it.    This wave current of depolarisation from B  to C is called as intracellular current. Now,   the same intracellular current will flow from cell  C to cell D, not only it goes in that direction,  

but it also displaces some of the positive ions  attached to the cell membrane in the cell D,   and that is called as capacitance current.  Now, these positive ions will flow from   cell C back to cell B in the opposite direction.  This is called as extracellular current.   

So, whenever there is an intracellular  current flowing from one cell to another,   an equivalent and opposite extracellular current  will be flowing in the reverse direction.   The flow of this extracellular current in the  heart, gives rise to an instantaneous vector  

in the heart, and this changes with time.  ECG is nothing but the sum of all these   electrical vectors which are recorded at one  particular plane and at one particular time.    So, the cardiac muscle fibres are actually, they  connected to each other in series and parallel.  

Their membranes form the intercalated  disc, which has got the gap junctions   across which the current freely flows  from one cell to another in one direction.   And hence, when one cell is excited,  the action potential can easily spread  

through the gap junctions. That is how when  one cardiac cell is excited, the entire cardiac   muscle will act like a syncytium and that is in a  unitary fashion. In fact, we have got one atrial   syncytium and one ventricular syncytium. That  is the importance of this gap junctions.   

Coming to the properties of the cardiac  muscle. They are excitability or bathmotropism,   conductivity or dromotropism, contractility or  inotropism, and rhythmicity or chronotropism;   along with that, we have got a special feature  of refractory period. Now, with respect to ECG,  

the first two properties, that is the  excitability and conductivity are very   important, and we will discuss about that.  Excitability is nothing but the ability of   the cardiac tissue to respond to stimuli by  producing an action potential. So, in that way,  

there are 2 types of cardiac tissues, excitable  cardiac tissues, which are: conducting tissue   which is producing a pacemaker potential; example  is the SA node; other one is a contractile tissue   which produces a true action potential as  seen in the ventricular myocardium.   

What is this pacemaker potential? Here,  spontaneous time dependent depolarisation occurs,   but the pacemaker cells show an unstable resting  membrane potential. The resting membrane potential   ranges from -65 to -55 millivolts. Now, why this  resting membrane potential is unstable? Because,  

there is slow rise of the resting membrane  potential because of the slow depolarisation.   This rising phase of the resting membrane  potential is called as prepotential.    So, when it rises slowly and when it reaches  -40 millivolts; this is the firing level;  

a rapid depolarisation will occur which goes  up to +5 millivolts, which will be followed by   rapid repolarisation. This completes one  action potential in a pacemaker tissue.    You can see here in this picture, SA nodal  potential is depicted. You can see the slope  

of rise in depolarization; from -60, gradually it  goes up to -40. When it reaches -40, that is that   firing level, it throws a depolarisation which  will be followed by a repolarisation, and again   the resting membrane potential is unstable, it  keeps on increasing until it reaches the next  

level, next cycle, that is -40 millivolts. The  similar picture is shown in the AV node.    Now, this slow rise in the depolarisation is  called as prepotential. What is the ionic basis   of this prepotential? This happens at the end of  repolarisation or sometimes hyperpolarization;  

that is why it is called as I h, that is,  hyperpolarising currents. Now, what happens   during the first half or early phases of this  prepotential, the potassium efflux is decreased;   the conductance of the potassium through  the potassium channels, it is decreased.   

Also, there occurs opening up of one particular  type of channels called as leaky sodium channels,   or it is otherwise called as funny channels,  because it allows both the sodium ions   and potassium ions. So, because of that,  there is slow entry of the positive ion,  

maybe sodium ion, that leads to slow rise in  the depolarisation. The latter half of the   prepotential is because of opening up of transient  type of calcium channels and calcium influx.    Once it reaches -40 millivolts, another type of  calcium channels is opened; that is, long lasting  

calcium channels, and there will be rapid inflow  of calcium ions. Remember, the SA nodal potential   and the AV nodal potential, the depolarisation is  because of opening up of calcium channels; sodium   channels has no role in pacemaker potential.  So, the unstable RMP, the early part is due to the  

hyperpolarising currents as well as the funny  currents, and the later part is because of   T type calcium channels. Rapid depolarisation  is because of L type calcium channels   and repolarisation is because  of potassium efflux.   

Look at this picture which shows the regulation  of the pacemaker activity by the sympathetic   and parasympathetic activation. See, this is  the normal rhythm of the pacemaker tissue.   When there is sympathetic stimulation,  look at the slope of this prepotential,  

it is increased. Now, why this occurs is, the  noradrenaline produced in the sympathetic nerves,   they act via the beta 1 receptors; it  increases the intracellular cyclic AMP;   this will open up the L type calcium channels; so,  rapidly this depolarisation will take place.   

That is why the slope is increased  and the heart rate is also increased.   Now, look at the vagal stimulation, look at  the slope here; slope of the prepotential is   decreased. Here, the acetylcholine released  at the vagal nerves increases the potassium  

conductance and slows the hyperpolarising  currents; also, via the M 2 receptors,   it delays the opening up of the calcium channels.  So, that is how it delays the next impulse.   So, this decreases the slope of the prepotential  and hence decreases the heart rate.   

Next we will see about the contractile tissue  potential; see, the atrial muscle as well as the   ventricular muscle. The one important feature that  you should notice is, look at the resting membrane   potential, it is a stable resting membrane  potential ranging from -85 to -90 millivolts. So,  

the baseline is a straight line, it is not a  slope unlike we saw in the pacemaker potential,   which will be followed by a rapid rise or a  straight depolarisation which crosses 0 potential.   And then, there will be a short repolarisation  which is followed by a plateau and then  

a regular repolarisation occurs until it reaches  the resting membrane potential level.    Now, this Purkinje fibre is almost similar  to the ventricular muscle in terms of the   electrical activity, but the only difference  is, look at the resting membrane potential;  

this is a pacemaker tissue, so, this shows  the unstable resting membrane potential;   you can see the slope. Whereas, in ventricular  muscle, it is stable; it is a straight line here.   But similar to the ventricular muscle, this  has also got a straight line denoting the  

depolarisation; that is, rapid depolarisation; an  initial rapid repolarisation followed by a plateau   and then the slow repolarisation.  This is because, in Purkinje fibres,   a depolarisation involves both the sodium channels  as well as the calcium channels, whereas in  

the pacemaker tissue, the depolarisation is  only because of the calcium channels.    So, the contractile tissue action  potential is created by the fast fibres,   especially the ventricular and the atrial  fibres. Resting membrane potential is  

stable and it has got various phases  as is depicted in this picture.   Phase 0 is the rapid depolarisation;  this is because of the sodium   currents. In phase 1 will be the initial rapid  repolarisation; this is because of the closure  

of the sodium channels as well as opening  up of the calcium channels. There will be   a plateau phase that is phase 2, which is done by  the slow influx of the calcium ions, which will be   followed by the repolarisation phase 3 and back  to the resting membrane potential phase 4.   

Summary of the ionic basis of cardiac action  potential: Phase 0 is because of the sodium influx   through the voltage gated sodium channels.  There will be some influx of calcium ions   via the slow calcium sodium channels also. Phase 1  will be because of closure of the sodium channels  

and opening up of specific type of  potassium channels called as I TO; that is,   transient outward currents of potassium.  Phase 2 is because of the slow influx of the   calcium ions through the calcium channels and  also slow efflux of the potassium ions. So,  

the membrane potential does not change,  it remains a plateau. Phase 3 and phase   4 is because of the efflux of the potassium ions  through various types of potassium channels.    The next important property is the conductivity.  This is nothing but the ability to conduct an  

action potential by sequential depolarisation  of the adjacent cells, how the action potential   is conducted from one cell to another. Almost  all the cells are capable of this property,   that is conductivity, only that the conduction  velocity differs. For example, the SA node and  

the AV node are the slowest conducting fibres  with a velocity of 0.05 metre per second.    Purkinje fibre system is the fastest conducting  system in the heart with a velocity of 4 metre per   second. Atrium, ventricle and bundle of His, they  conduct at a velocity of 1 metre per second.   

This is the conduction pathway. As we all  know, SA node generates the potential,   it transmits to the AV node via the internodal  tract to the right atrium and via a branch of   anterior internodal tract to the left atrium. So,  within this 0.1 second, the entire right atrium  

and the left atrium is excited. And then, when the  impulse come to the AV node, there will be a delay   of about 0.1 second in the AV node.  Then, the impulses crosses the AV node,   goes to the bundle of His, its branches,  and then reaches the Purkinje system  

to excite the entire ventricular myocardium.  So, this takes around 0.08 to 0.1 second. So,   within approximately 0.3 second, the entire  heart atria and the ventricle gets excited   once the pacemaker potential is generated.  Now, what is this AV nodal delay? This is one  

important phenomenon happening in the AV node.  Here, the conduction of the rapid impulses   will be delayed for about 0.1 second in the AV  node. This is called as detrimental contraction.   Reason for this delay is that the transitional  fibres which connect the internodal tracts to  

the AV node are very small and they  have very slow conduction velocity,   even less than the SA node and the AV node; say  for example, 0.02 to 0.05 metre per second.    And they also have very few gap junctions. We know  that the atria and the ventricle are separated by  

a fibrous ring of tissue and this AV node and  the bundle of His and its branches are the only   way to transmit the impulses. And the advantage  of this AV nodal delay is that, because of this   delay only, the atrium is able to completely  contract and empty its blood into the ventricle  

before the ventricular contraction stops.  A sufficient amount of cardiac output is   possible only because of this AV nodal delay.  Now, this AV nodal delay is also shortened by   the sympathetic stimulation and lengthened  by the parasympathetic stimulation.   

So, once again, this picture  showing the SA node, AV node;   conduction occurs through the internodal tracts;  and from the AV node, bundle of His continues;   it transfers a short distance in the  septum, upper part of the septum,  

divides into right branch and the left branch; the  left branch again divides into anterior fascicle   and the posterior fascicle; and both the branches  run down the septum and merges with the Purkinje   fibre system. Now, how this  excitation wave spreads?   

We will see in this picture, this is the  beginning of the atrial excitation which is,   the excitation produced in the SA node is  travelling towards the AV node. And in this   picture, as shown in this yellowish coloration,  both the right atrium and the left atrium is  

excited. That means, atrial excitation is  complete. You can see the recording of this   action potential, here in the bottom picture.  When the atrium started its impulse generation,   a slight upward deflection has started. And when  both the atrium are conducted, there is a complete  

one positive wave. This wave is the P wave of  ECG. Next, the ventricle is getting excited. So,   when the impulse comes to the bundle of His,  which is present in the top of the septum, it goes   towards the left side little bit, and then, in the  mid of the septum, it turns towards the right side  

and the spread of excitation goes downwards  towards apex of the ventricle and then turns   upwards on either side towards the AV groove.  So, that is how the complete ventricular   myocardium gets excited. You can see, during the  septal activation, there is a formation of some  

negative wave which will be followed by a positive  wave. And then, when the ventricular excitation is   complete, you can see 3 wave forms, Q wave, R wave  and S wave. Together, we call it as QRS complex.   That is denoting the ventricular excitation.  This excitation spreads from endocardium to  

epicardium; that is very important. Now, next  is the ventricular relaxation which is occurring   from epicardium to endocardium, and that forms  another positive wave called as T wave.    So, once the depolarisation comes to the AV  node and goes to the bundle of His, it starts  

at the left side of the septum and moves to the  right, across the mid portion of the septum. Then,   the excitation spreads down the septum  to the apex and turns along the walls of   the ventricles on both sides, right and left  side, and goes towards the AV groove, from the  

endocardium to the epicardial surface.  The last portion of the heart to get   excited is the posterobasal portion of the  left ventricle, the pulmonary conus and the   uppermost part of the septum. This is how  the spread of excitation takes place.   

So, this is a picture showing the depolarisation  or the action potential produced at different   parts of the conducting system. So, this is  the SA nodal potential, you can see here;   then is the atrial muscle; then the AV  node; then the His bundle; its branches;  

Purkinje fibre system; finally, the  ventricular muscle. Now, ECG is nothing but   the sum of all these action potential at  any given time on any given plane.    So, this electrical vector of all the  action potentials produced in different  

conducting systems of the heart gives rise  to ECG and its various waveforms namely P   wave, QRS complex, T wave and U wave.  Summarising the entire content, we have seen   that the conducting system of the heart includes  the cardiac cells classified as different ways  

based on the function as pacemaker cells and  the contractile cells, and based on their speed   of conduction as slow fibres and fast fibres.  Pacemaker cells are SA node, AV node, bundle   of His, branches, Purkinje fibres. Contractile  cells are atrial and ventricular myocytes.   

Slow fibres are SA node and AV node, whereas  other cells are fast fibres. Next, we saw about   the production of this extracellular current; that  is, when the action potential or when the wave of   depolarisation spreads from one cell to another  cell as intracellular current, an equivalent  

wave of depolarisation will spread in  the opposite direction. This forms the   extracellular electrical vector.  And the ECG is nothing but sum of all   these electrical vectors recorded at one  particular plane at one particular point.  

And we saw that the conduction pathway is  complete within 0.3 seconds since its origin at   SA node and there is a delay of this 0.1 second  in the AV node, which is actually beneficial   for producing a better cardiac output and  better contraction. We also saw how the wave  

of excitation spreads across the different  parts of the conducting tissue, starting   from the SA node and then the entire atrium,  right and the left atrium gets excited, that   leads on to a positive wave that is P wave.  Then comes the wave of excitation along the septum  

and the ventricle muscle, and that completes  the QRS complex, followed by the ventricular   relaxation which gives rise to the T wave. This is  a picture finally showing the electrical activity,   that is, depolarisation and repolarisation pattern  in different parts of the conducting system, right  

from the SA node till the ventricular muscle.  And the sum of all these electrical activities   in terms of action potential is recorded as  different waveforms of ECG. So, we will be   discussing a lot more about ECG in the further  lectures. I thank our university, Chettinad  

Academy of Research and Education and NPTEL for  enabling this course to the viewers. Thank you.